Muscles &Muscle Tissue Chapter 10
Functions of Skeletal Muscles Produce skeletal movement Maintain body position Support soft tissues Guard body openings Maintain body temperature
Functional Characteristics of Muscle Excitability (irritability) Can receive and respond to stimuli. Stimuli can include nerve impulses, stretch, hormones or changes in the chemical environment. Contractility – the ability to shorten with increasing tension. Extensibility – the ability to stretch. Elasticity – the ability to snap back (recoil) to their resting length after being stretched.
Three types of muscle Skeletal Smooth Cardiac
Characteristics of Skeletal Muscle Striated Multinucleate (it is a syncytium) Voluntary Parallel fibers
Organization of Connective Tissues Figure 10–1
Formation of Skeletal Muscle Fibers Skeletal muscle cells are called fibers Formation of Skeletal Muscle Fibers
Organization of Skeletal Muscle Fibers
Anatomy of a myofibril
A Triad Is formed by 1 T tubule and 2 terminal cisternae
Sarcomeres Figure 10–4
Muscle Striations A striped or striated pattern within myofibrils: alternating dark, thick filaments (A bands) and light, thin filaments (I bands)
M Lines and Z Lines M line: Z lines: the center of the A band at midline of sarcomere Z lines: the centers of the I bands at 2 ends of sarcomere
Zone of Overlap The densest, darkest area on a light micrograph Where thick and thin filaments overlap
The H Zone The area around the M line Has thick filaments but no thin filaments
Titin Are strands of protein Reach from tips of thick filaments to the Z line Stabilize the filaments
Sarcomere Structure
Summary of skeletal muscle anatomy: muscles are made of fascicles
Fascicles are made of fibers, fibers are made of myofibrils
Level 1: Skeletal Muscle Figure 10–6 (1 of 5)
Level 2: Muscle Fascicle Figure 10–6 (2 of 5)
Level 3: Muscle Fiber Figure 10–6 (3 of 5)
Level 4: Myofibril Figure 10–6 (4 of 5)
Level 5: Sarcomere Figure 10–6 (5 of 5)
Fibrils are divided into sarcomeres, sarcomeres are made of myofilaments
Myofilaments are made of protein molecules
A Thin Filament
4 Thin Filament Proteins F actin: is 2 twisted rows of globular G actin the active sites on G actin strands bind to myosin
4 Thin Filament Proteins Nebulin: holds F actin strands together
4 Thin Filament Proteins Tropomyosin: is a double strand prevents actin–myosin interaction
4 Thin Filament Proteins Troponin: a globular protein binds tropomyosin to G actin controlled by Ca2+
Troponin and Tropomyosin Figure 10–7b
A Thick Filament Figure 10–7c
Thick Filaments Contain twisted myosin subunits Contain titin strands that recoil after stretching
The Mysosin Molecule Figure 10–7d
Muscle Contraction: the Sliding Filament Theory Muscle contraction requires: Stimulus – the generation of an action potential. Crossbridge formation – interaction between the thick and thin myofilaments. This is triggered by Ca++ ions released from the sarcoplasmic reticulum. Energy – ATP to energize the myosin molecules.
Sliding Filaments
Skeletal Muscle Contraction
T- tubules supply the stimulus, Sarcoplasmic Reticulum supplies the Ca++, Mitochondria supply the ATP.
The Process of Contraction Neural stimulation of sarcolemma: causes excitation–contraction coupling Cisternae of SR release Ca2+: which triggers interaction of thick and thin filaments consuming ATP and producing tension
Skeletal Muscle Innervation
Skeletal Muscle Innervation Figure 10–10c
The Neuromuscular Junction Is the location of neural stimulation Action potential (electrical signal): travels along nerve axon ends at synaptic terminal
A neuromuscular junction (NMJ).
acetylcholine The actual synapse
Synaptic Terminal Releases neurotransmitter (acetylcholine or ACh) Into the synaptic cleft (gap between synaptic terminal and motor end plate)
The Neurotransmitter Acetylcholine or ACh: travels across the synaptic cleft binds to membrane receptors on sarcolemma (motor end plate) causes sodium–ion rush into sarcoplasm is quickly broken down by enzyme (acetylcholinesterase or AChE)
Action Potential Generated by increase in sodium ions in sarcolemma Travels along the T tubules Leads to excitation–contraction coupling
Excitation–Contraction Coupling Action potential reaches a triad: releasing Ca2+ triggering contraction Requires myosin heads to be in “cocked” position: loaded by ATP energy
Exposing the Active Site
The Contraction Cycle
The Contraction Cycle
The Contraction Cycle
The Contraction Cycle
5 Steps of the Contraction Cycle Exposure of active sites Formation of cross-bridges Pivoting of myosin heads Detachment of cross-bridges Reactivation of myosin
Show the animation
A Review of Muscle Contraction
Excitation-Contraction coupling Stimulus or excitation is required for muscles to contract. In skeletal muscle, the stimulus is from a motor neuron. The stimulus is in the form of an action potential. This action potential starts at the neuromuscular junction (NMJ).
Excitation-contraction coupling
Show NMJ animation
Micrograph of an NMJ
A Synapse Synaptic vesicles
Tension and Sarcomere Length Figure 10–14
Length–Tension Relationship Number of pivoting cross-bridges depends on: amount of overlap between thick and thin fibers Optimum overlap produces greatest amount of tension: too much or too little reduces efficiency
Length–Tension Relationship Normal resting sarcomere length: is 75% to 130% of optimal length
Frequency of Stimulation A single neural stimulation produces: a single contraction or twitch which lasts about 7–100 msec Sustained muscular contractions: require many repeated stimuli
Tension in a Twitch Length of twitch depends on type of muscle
Myogram A graph of twitch tension development Figure 10–15b (Navigator)
3 Phases of Twitch Latent period before contraction: the action potential moves through sarcolemma causing Ca2+ release
3 Phases of Twitch Contraction phase: calcium ions bind tension builds to peak
3 Phases of Twitch Relaxation phase: Ca2+ levels fall active sites are covered tension falls to resting levels
Treppe A stair-step increase in twitch tension Figure 10–16a
Treppe Repeated stimulations immediately after relaxation phase: stimulus frequency < 50/second Causes a series of contractions with increasing tension
Wave Summation Increasing tension or summation of twitches
Wave Summation Repeated stimulations before the end of relaxation phase: stimulus frequency > 50/second Causes increasing tension or summation of twitches
Incomplete Tetanus Twitches reach maximum tension Figure 10–16c
Incomplete Tetanus If rapid stimulation continues and muscle is not allowed to relax, twitches reach maximum level of tension
Complete Tetanus Figure 10–16d
Complete Tetanus If stimulation frequency is high enough, muscle never begins to relax, and is in continuous contraction
Comparative speed of different muscles
Tension Produced by Whole Skeletal Muscles Depends on: internal tension produced by muscle fibers external tension exerted by muscle fibers on elastic extracellular fibers total number of muscle fibers stimulated
Motor Units in a Skeletal Muscle Figure 10–17
Motor Units in a Skeletal Muscle Contain hundreds of muscle fibers That contract at the same time Controlled by a single motor neuron
Recruitment (Multiple Motor Unit Summation) In a whole muscle or group of muscles, smooth motion and increasing tension is produced by slowly increasing size or number of motor units stimulated
Maximum Tension Achieved when all motor units reach tetanus Can be sustained only a very short time
Sustained Tension Less than maximum tension Allows motor units to rest in rotation
2 Types of Skeletal Muscle Tension Isotonic contraction Isometric contraction
Isotonic Contraction Figure 10–18a, b
Isotonic Contraction Skeletal muscle changes length: resulting in motion If muscle tension > resistance: muscle shortens (concentric contraction) If muscle tension < resistance: muscle lengthens (eccentric contraction)
Isometric Contraction Figure 10–18c, d
Isometric Contraction Skeletal muscle develops tension, but is prevented from changing length Note: Iso = same, metric = measure
Resistance and Speed of Contraction
Resistance and Speed of Contraction Are inversely related The heavier the resistance on a muscle: the longer it takes for shortening to begin and the less the muscle will shorten
ATP and Muscle Contraction Sustained muscle contraction uses a lot of ATP energy Muscles store enough energy to start contraction Muscle fibers must manufacture more ATP as needed
ATP and CP Reserves Adenosine triphosphate (ATP): the active energy molecule Creatine phosphate (CP): the storage molecule for excess ATP energy in resting muscle
Recharging ATP Energy recharges ADP to ATP: using the enzyme creatine phosphokinase (CPK) When CP is used up, other mechanisms generate ATP
Energy Storage in Muscle Fiber Table 10–2
ATP Generation Cells produce ATP in 2 ways: aerobic metabolism of fatty acids in the mitochondria anaerobic glycolysis in the cytoplasm
Aerobic Metabolism Is the primary energy source of resting muscles Breaks down fatty acids Produces 34 ATP molecules per glucose molecule
Anaerobic Glycolysis Is the primary energy source for peak muscular activity Produces 2 ATP molecules per molecule of glucose Breaks down glucose from glycogen stored in skeletal muscles
Anaerobic Metabolism: a losing proposition
Energy Use and Muscle Activity At peak exertion: muscles lack oxygen to support mitochondria muscles rely on glycolysis for ATP pyruvic acid builds up, is converted to lactic acid
Muscle Metabolism
Muscle Metabolism Figure 10–20b
Muscle Metabolism Figure 10–20c
Results of Muscle Fatigue Depletion of metabolic reserves Damage to sarcolemma and sarcoplasmic reticulum Low pH (lactic acid) Muscle exhaustion and pain
The Recovery Period The time required after exertion for muscles to return to normal Oxygen becomes available Mitochondrial activity resumes
The Cori Cycle The removal and recycling of lactic acid by the liver Liver converts lactic acid to pyruvic acid Glucose is released to recharge muscle glycogen reserves
Oxygen Debt After exercise: the body needs more oxygen than usual to normalize metabolic activities resulting in heavy breathing
Muscle Performance Power: Endurance: Power and endurance depend on: the maximum amount of tension produced Endurance: the amount of time an activity can be sustained Power and endurance depend on: the types of muscle fibers physical conditioning
3 Types of Skeletal Muscle Fibers Fast fibers Slow fibers Intermediate fibers
Fast Fibers Contract very quickly Have large diameter, large glycogen reserves, few mitochondria Have strong contractions, fatigue quickly
Slow Fibers Are slow to contract, slow to fatigue Have small diameter, more mitochondria Have high oxygen supply Contain myoglobin (red pigment, binds oxygen)
Intermediate Fibers Are mid-sized Have low myoglobin Have more capillaries than fast fiber, slower to fatigue
Fast versus Slow Fibers Figure 10–21
Comparing Skeletal Muscle Fibers
Muscles and Fiber Types White muscle: mostly fast fibers pale (e.g., chicken breast) Red muscle: mostly slow fibers dark (e.g., chicken legs) Most human muscles: mixed fibers pink
Muscle Hypertrophy Muscle growth from heavy training: increases diameter of muscle fibers increases number of myofibrils increases mitochondria, glycogen reserves
Muscle Atrophy Lack of muscle activity: reduces muscle size, tone, and power
Structure of Cardiac Tissue Cardiac muscle is striated, found only in the heart Figure 10–22
7 Characteristics of Cardiocytes Unlike skeletal muscle, cardiac muscle cells (cardiocytes): are small have a single nucleus have short, wide T tubules
7 Characteristics of Cardiocytes have no triads have SR with no terminal cisternae are aerobic (high in myoglobin, mitochondria) have intercalated discs
Intercalated Discs Are specialized contact points between cardiocytes Join cell membranes of adjacent cardiocytes (gap junctions, desmosomes)
Functions of Intercalated Discs Maintain structure Enhance molecular and electrical connections Conduct action potentials
Coordination of Cardiocytes Because intercalated discs link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells
4 Functions of Cardiac Tissue Automaticity: contraction without neural stimulation controlled by pacemaker cells Variable contraction tension: controlled by nervous system
4 Functions of Cardiac Tissue Extended contraction time Prevention of wave summation and tetanic contractions by cell membranes
Structure of Smooth Muscle Nonstriated tissue Figure 10–23
Comparing Smooth and Striated Muscle Different internal organization of actin and myosin Different functional characteristics
8 Characteristics of Smooth Muscle Cells Long, slender, and spindle shaped Have a single, central nucleus Have no T tubules, myofibrils, or sarcomeres Have no tendons or aponeuroses
8 Characteristics of Smooth Muscle Cells Have scattered myosin fibers Myosin fibers have more heads per thick filament Have thin filaments attached to dense bodies Dense bodies transmit contractions from cell to cell
Functional Characteristics of Smooth Muscle Excitation–contraction coupling Length–tension relationships Control of contractions Smooth muscle tone
Excitation–Contraction Coupling Free Ca2+ in cytoplasm triggers contraction Ca2+ binds with calmodulin: in the sarcoplasm activates myosin light chain kinase Enzyme breaks down ATP, initiates contraction
Length–Tension Relationships Thick and thin filaments are scattered Resting length not related to tension development Functions over a wide range of lengths (plasticity)
Control of Contractions Subdivisions: multiunit smooth muscle cells: connected to motor neurons visceral smooth muscle cells: not connected to motor neurons rhythmic cycles of activity controlled by pacesetter cells
Smooth Muscle Tone Maintains normal levels of activity Modified by neural, hormonal, or chemical factors
Smooth Muscle
Varicosities
Skeletal Smooth Diameter 10 - 100 m 3 - 8 m Connective tissue Epi-, Peri- & Endomysium Endomysium only SR Yes, complex Barely, simple T - tubules yes no Sarcomeres Gap Junctions voluntary Neurotransmitters Acetylcholine (Ach) Ach, epinephrine, norepinephrine, et al Regeneration Very little Lots, for muscle
Future governors of Califorina?